Exposure of tumor necrosis factor-α to luminal membrane of bovine brain capillary endothelial cells cocultured with astrocytes induces a delayed increase of permeability and cytoplasmic stress fiber formation of actin

M. Deli, L. Descamps, M. P. Dehouck, R. Cecchelli, F. Joo, C. Ábrahám, G. Torpier

Research output: Contribution to journalArticle

129 Citations (Scopus)

Abstract

Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, has long been known to be involved in the pathogenesis of central nervous system infections and of certain neurodegenerative diseases. However, the possible role of the blood-brain barrier (BBB), the active interface between the blood circulation and brain tissue, remained unknown during these pathological conditions. In our in vitro reconstructed BBB model, 1-hr exposure of recombinant human TNF-α (in concentrations of 50, 250, and 500 U/ml, respectively) to the luminal membrane of bovine brain capillary endothelial cells (BBCEC) did not change significantly the transendothelial flux of either sucrose (m.w. 342 Da), or inulin (m.w. 5 kDa) up to 4 hr (early phase), except for a slight decrease (P <0.05) in sucrose permeation at 2-4 hr with the highest dose of TNF-α. On the other hand, at 16 hr after the 1- hr challenge with TNF-α (delayed phase) at all 3 concentrations, significant increase was induced in the permeability of BBCEC monolayers for both markers. These changes of permeability were accompanied by a selective reorganization of F-actin filaments into stress fibers, while the intracellular distribution of vimentin remained similar to the control. These results suggest that BBCEC can respond directly to TNF-α by a delayed increase of permeability and reorganization of actin filaments.

Original languageEnglish
Pages (from-to)717-726
Number of pages10
JournalJournal of Neuroscience Research
Volume41
Issue number6
DOIs
Publication statusPublished - 1995

Fingerprint

Stress Fibers
Astrocytes
Actins
Permeability
Endothelial Cells
Tumor Necrosis Factor-alpha
Membranes
Brain
Blood-Brain Barrier
Actin Cytoskeleton
Sucrose
Central Nervous System Infections
Inulin
Blood Circulation
Vimentin
Neurodegenerative Diseases
Cytokines

Keywords

  • actin
  • astrocytes
  • blood-brain barrier (BBB)
  • endothelial cells
  • stress fiber
  • tumor necrosis factor-α
  • vascular permeability

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

@article{5e5d194d80c546eaabed39ea8732b9ec,
title = "Exposure of tumor necrosis factor-α to luminal membrane of bovine brain capillary endothelial cells cocultured with astrocytes induces a delayed increase of permeability and cytoplasmic stress fiber formation of actin",
abstract = "Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, has long been known to be involved in the pathogenesis of central nervous system infections and of certain neurodegenerative diseases. However, the possible role of the blood-brain barrier (BBB), the active interface between the blood circulation and brain tissue, remained unknown during these pathological conditions. In our in vitro reconstructed BBB model, 1-hr exposure of recombinant human TNF-α (in concentrations of 50, 250, and 500 U/ml, respectively) to the luminal membrane of bovine brain capillary endothelial cells (BBCEC) did not change significantly the transendothelial flux of either sucrose (m.w. 342 Da), or inulin (m.w. 5 kDa) up to 4 hr (early phase), except for a slight decrease (P <0.05) in sucrose permeation at 2-4 hr with the highest dose of TNF-α. On the other hand, at 16 hr after the 1- hr challenge with TNF-α (delayed phase) at all 3 concentrations, significant increase was induced in the permeability of BBCEC monolayers for both markers. These changes of permeability were accompanied by a selective reorganization of F-actin filaments into stress fibers, while the intracellular distribution of vimentin remained similar to the control. These results suggest that BBCEC can respond directly to TNF-α by a delayed increase of permeability and reorganization of actin filaments.",
keywords = "actin, astrocytes, blood-brain barrier (BBB), endothelial cells, stress fiber, tumor necrosis factor-α, vascular permeability",
author = "M. Deli and L. Descamps and Dehouck, {M. P.} and R. Cecchelli and F. Joo and C. {\'A}brah{\'a}m and G. Torpier",
year = "1995",
doi = "10.1002/jnr.490410602",
language = "English",
volume = "41",
pages = "717--726",
journal = "Journal of Neuroscience Research",
issn = "0360-4012",
publisher = "Wiley-Liss Inc.",
number = "6",

}

TY - JOUR

T1 - Exposure of tumor necrosis factor-α to luminal membrane of bovine brain capillary endothelial cells cocultured with astrocytes induces a delayed increase of permeability and cytoplasmic stress fiber formation of actin

AU - Deli, M.

AU - Descamps, L.

AU - Dehouck, M. P.

AU - Cecchelli, R.

AU - Joo, F.

AU - Ábrahám, C.

AU - Torpier, G.

PY - 1995

Y1 - 1995

N2 - Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, has long been known to be involved in the pathogenesis of central nervous system infections and of certain neurodegenerative diseases. However, the possible role of the blood-brain barrier (BBB), the active interface between the blood circulation and brain tissue, remained unknown during these pathological conditions. In our in vitro reconstructed BBB model, 1-hr exposure of recombinant human TNF-α (in concentrations of 50, 250, and 500 U/ml, respectively) to the luminal membrane of bovine brain capillary endothelial cells (BBCEC) did not change significantly the transendothelial flux of either sucrose (m.w. 342 Da), or inulin (m.w. 5 kDa) up to 4 hr (early phase), except for a slight decrease (P <0.05) in sucrose permeation at 2-4 hr with the highest dose of TNF-α. On the other hand, at 16 hr after the 1- hr challenge with TNF-α (delayed phase) at all 3 concentrations, significant increase was induced in the permeability of BBCEC monolayers for both markers. These changes of permeability were accompanied by a selective reorganization of F-actin filaments into stress fibers, while the intracellular distribution of vimentin remained similar to the control. These results suggest that BBCEC can respond directly to TNF-α by a delayed increase of permeability and reorganization of actin filaments.

AB - Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, has long been known to be involved in the pathogenesis of central nervous system infections and of certain neurodegenerative diseases. However, the possible role of the blood-brain barrier (BBB), the active interface between the blood circulation and brain tissue, remained unknown during these pathological conditions. In our in vitro reconstructed BBB model, 1-hr exposure of recombinant human TNF-α (in concentrations of 50, 250, and 500 U/ml, respectively) to the luminal membrane of bovine brain capillary endothelial cells (BBCEC) did not change significantly the transendothelial flux of either sucrose (m.w. 342 Da), or inulin (m.w. 5 kDa) up to 4 hr (early phase), except for a slight decrease (P <0.05) in sucrose permeation at 2-4 hr with the highest dose of TNF-α. On the other hand, at 16 hr after the 1- hr challenge with TNF-α (delayed phase) at all 3 concentrations, significant increase was induced in the permeability of BBCEC monolayers for both markers. These changes of permeability were accompanied by a selective reorganization of F-actin filaments into stress fibers, while the intracellular distribution of vimentin remained similar to the control. These results suggest that BBCEC can respond directly to TNF-α by a delayed increase of permeability and reorganization of actin filaments.

KW - actin

KW - astrocytes

KW - blood-brain barrier (BBB)

KW - endothelial cells

KW - stress fiber

KW - tumor necrosis factor-α

KW - vascular permeability

UR - http://www.scopus.com/inward/record.url?scp=0029126861&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029126861&partnerID=8YFLogxK

U2 - 10.1002/jnr.490410602

DO - 10.1002/jnr.490410602

M3 - Article

VL - 41

SP - 717

EP - 726

JO - Journal of Neuroscience Research

JF - Journal of Neuroscience Research

SN - 0360-4012

IS - 6

ER -